Piceatannol is a natural
plant-derived compound with protective effects against
cardiovascular diseases. However, its effect on cerebral ischaemia-
reperfusion injury (CIRI) induced by oxidative stress remains unclear. This study aimed to investigate
piceatannol's antioxidation in CIRI. An in vitro
oxygen-
glucose deprivation followed by reoxygenation model was used and cell viability was measured. A
middle cerebral artery occlusion followed by reperfusion model was used in vivo. Neurological function, encephalisation quotient, oedema, and volume of the
cerebral infarction were then evaluated. The effects of
piceatannol on histopathological findings, as well as the ultrastructure of the cortex, were analysed. The activity of
superoxide dismutase (SOD),
glutathione peroxidase (GSH-Px), and
lactate dehydrogenase (LDH) and the
malondialdehyde (MDA) content was measured both in vitro and in vivo. Finally, the expression of nuclear factor erythroid-2-related factor 2 (Nrf2), hemeoxygenase-1 (HO-1), and
nicotinamide adenine dinucleotide phosphate quinone oxidoreductase 1 (NQO1) in cerebral tissue was detected using reverse transcription quantitative polymerase chain reaction (RT-qPCR) and western blotting. Our results demonstrated that cell viability in the
piceatannol groups was increased. The SOD, GSH-Px activities were increased as LDH activity and MDA content decreased in the
piceatannol groups both in vitro and in vivo, reflecting a decrease in oxidative stress. The neurological severity score and
infarction volume in the
piceatannol groups at doses of 10 and 20 mg/kg were lower than those of the model group. Furthermore, the damage seen on histopathological examination was partially attenuated by
piceatannol. RT-qPCR and western blot analysis indicated that the expression of Nrf2, HO-1, and NQO1 were significantly increased by
piceatannol. The results of the study demonstrate that
piceatannol exerts a protective effect against CIRI.